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Updated: Sep 4, 2025

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
Silencing lncRNA 93358 Inhibits the Apoptosis of Myocardial Cells in Myocardial Infarction Rats by Inducing the
Jiumei Cai1,2,3, Xiaoping Wang2, Wei Liao2
1The Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong 510515, China.
Objective:
To explore the inhibitor effects and mechanism of lncRNA 93358 against the apoptosis of myocardial cells in rats with myocardial infarction.
Methods:
The myocardial infarction model was established in rats, which were identified by cardiac ultrasound. TTC staining was used to evaluate the degree of heart infarction, and HE staining was utilized to determine the pathological state in myocardial tissues. The apoptotic state in myocardial tissues was confirmed by TUNEL assay. lncRNA 93358 was screened out using a high-throughput sequencing which was confirmed by RT-qPCR. The interaction between miR-466c-3p and SLC8A1 was identified using the dual-luciferase reporter assay. The expression level of Bax, Bcl-2, and SLC8A1 was determined in lncRNA 93358 knockdown cells using RT-qPCR and Western blotting.
Results:
Massive myocardial necrosis was observed in model rats according to the results of TTC staining, HE staining, and TUNEL assay. lncRNA 93358 and Bax were found significantly upregulated, and Bcl-2 and SLC8A1 were greatly downregulated in model rats, which were dramatically reversed by the knockdown of lncRNA 93358, accompanied by the decline area of myocardial necrosis and decreased apoptotic myocardial cells.
Conclusion:
Silencing lncRNA 93358 inhibits the apoptosis of myocardial cells in rats with myocardial infarction by inducing the expression of SLC8A1.
Insights
Silencing long non-coding RNA 93358 (lncRNA 93358) inhibits myocardial cell apoptosis in myocardial infarction (MI) rat models. This protective effect is mediated by inducing the expression of solute carrier family 8 member A1 (SLC8A1).
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- RNA Biology
Background:
- Myocardial infarction (MI) is a leading cause of mortality.
- Apoptosis of myocardial cells exacerbates cardiac dysfunction post-MI.
- Identifying novel therapeutic targets to mitigate myocardial cell death is crucial.
Purpose of the Study:
- To investigate the inhibitory effects and mechanism of long non-coding RNA 93358 (lncRNA 93358) on myocardial cell apoptosis in a rat model of myocardial infarction.
- To elucidate the role of lncRNA 93358 in regulating cell death pathways and its potential as a therapeutic target.
Main Methods:
- Establishment of a rat model of myocardial infarction, confirmed by echocardiography.
- Assessment of infarct size and myocardial pathology using TTC and HE staining.
- Evaluation of myocardial cell apoptosis via TUNEL assay.
- Identification and validation of lncRNA 93358 expression using high-throughput sequencing and RT-qPCR.
- Investigation of the interaction between lncRNA 93358, miR-466c-3p, and SLC8A1 using dual-luciferase reporter assays.
- Analysis of apoptosis-related protein and SLC8A1 expression (Bax, Bcl-2, SLC8A1) through RT-qPCR and Western blotting following lncRNA 93358 knockdown.
Main Results:
- Myocardial infarction model rats exhibited significant myocardial necrosis, increased lncRNA 93358 and Bax expression, and decreased Bcl-2 and SLC8A1 levels.
- Knockdown of lncRNA 93358 significantly reversed these changes, reducing infarct size and myocardial apoptosis.
- lncRNA 93358 knockdown led to increased SLC8A1 expression, suggesting its role in the protective mechanism.
Conclusions:
- Silencing lncRNA 93358 demonstrates a protective effect against myocardial cell apoptosis in a rat model of myocardial infarction.
- The mechanism involves the induction of solute carrier family 8 member A1 (SLC8A1) expression.
- lncRNA 93358 represents a potential therapeutic target for managing myocardial infarction by inhibiting apoptosis.
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